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Statin Dose-Response Lab (2D)

2D pharmacokinetic model of statin therapy: a one-compartment oral PK model drives plasma drug concentration, a Hill equation converts it into HMG-CoA reductase inhibition, and hepatic LDL kinetics respond over simulated days.

Medicine & Biophysics2DAdvanced60 FPS📱 Mobile-adapted⇄ 3D version

This 2D companion drives the same one-compartment PK model, Hill-equation enzyme inhibition and first-order LDL kinetics as the 3D lab, drawn as a flat schematic instead of an orbitable scene: a gut depot feeds a bloodstream loop, a liver icon spins its HMG-CoA reductase gate faster when unblocked, LDL particles flow along the loop in proportion to circulating LDL-C, and a live chart traces the LDL-C curve settling to a new steady state as the statin, dose and patient metabolism you choose take effect.

⚙ Under the hood

One-compartment oral PK model (dA/dt = −ka·A, dC/dt = ka·A/Vd − ke·C) feeds a Hill-equation HMG-CoA reductase inhibition term, which drives first-order LDL kinetics toward a new steady state — the same equations as the 3D lab, rendered as a 2D schematic with a live LDL-C chart.

PharmacokineticsHill EquationStatinsHMG-CoA ReductaseLDL CholesterolDose-Response

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

What determines how fast LDL cholesterol falls after starting a statin?

Three things: the statin's absorption/elimination rates (which set how much drug reaches the liver), the Hill-equation potency (IC50) that converts plasma concentration into HMG-CoA reductase inhibition, and the LDL turnover rate, which determines how quickly circulating LDL-C drifts toward its new, lower steady state once synthesis slows.

Why do higher doses show diminishing returns?

The Hill equation saturates: inhibition approaches an Imax ceiling as plasma concentration rises far past IC50, so doubling the dose well above that point adds little extra enzyme blockade even though plasma concentration keeps climbing.